ADVANCED DIGESTIVE ENDOSCOPY: ERCP - PART 6 docx

acute and chronic pancreatitis [27–29] (Figs 9.3 and 9.4). Unlike for biliary strictures, it may often be necessary to bridge the main pancreatic duct beyond the point of disruption with a stent in order to obtain closure of a pancreatic duct leak, especially if there is a small-caliber, diseased, or strictured pancreatic duct. CHAPTER 9206 Fig. 9.3 CT scan showing a persistent leak from the pancreatic duct after surgical debridement of severe necrotizing medication- induced pancreatitis. Fig. 9.4 ERCP showing bridging of the disrupted main pancreatic duct with a guidewire and stent, leading to ultimate closure of the leak. This is trial version www.adultpdf.com The use of transpapillary pancreatic duct stenting in evolving acute necrosis or complicated pancreatitis has been recently reported [30]. This is based on the theory that main pancreatic ductal disruption is integral to the pathophysiology of acute pancreatic necrosis, and suggests that transpapillary pancreatic stent- ing might be beneficial in the course of this difficult group of patients by reliev- ing downstream obstruction and thus reducing complications. In patients with pancreatic necrosis in various stages of evolution at the time of transfer to their institution, this group reported a management strategy including ERCP, with findings of main pancreatic duct disruptions in two-thirds of patients who were treated with transpapillary pancreatic stent plus/minus biliary sphincterotomy. In general, organized necrosis or fluid collections were drained separately by surgical, percutaneous, or endoscopic routes. They reported a very low mortal- ity in this case series of over 100 patients. Although an intriguing concept, this approach deserves further study in a randomized controlled trial. Special con- cerns with performance of ERCP in the setting of acute necrosis include the risk of introducing infection into otherwise sterile pancreatic necrosis and/or fluid collections. Smoldering pancreatitis Rapid resolution of persistent smoldering pancreatitis without associated pan- creatic duct disruption has been reported to occur with placement of a trans- papillary stent. We and others have also found this to be quite effective in patients with a prolonged course of smoldering pancreatitis that persists for 2 to 3 weeks or more, with pain and hyperamylasemia despite fasting and total par- enteral nutrition, and often without significant pancreatic injury evident by CT scan. Regardless of the etiology of pancreatitis, placement of a transpapillary stent can often interrupt and hasten resolution of the process [31,32]. There are limited data supporting this approach, with no randomized controlled trials. Acute recurrent pancreatitis Acute recurrent pancreatitis is most commonly the result of alcohol or gallstone disease. Other etiologies include medications such as azathioprine, tetracycline, or estrogens [33–35]. Metabolic causes such as severe hypertriglyceridemia [36] or hypercalcemia may be revealed by laboratory investigation. ‘Idiopathic’ pancreatitis Some 10–30% of patients with acute recurrent pancreatitis may have no etio- logy apparent by history, laboratory, and non-invasive imaging studies such as CT or ultrasound. Such patients are often labeled as having ‘idiopathic’ ERCP IN ACUTE PANCREATITIS 207 This is trial version www.adultpdf.com pancreatitis. ‘Unexplained acute pancreatitis’ and ‘unexplained acute recurrent pancreatitis’ are more appropriate terms, reserving the label ‘idiopathic’ for pancreatitis whose etiology remains unidentified after a truly exhaustive and advanced evaluation. Advanced diagnostic investigation may reveal etiologies such as microlithiasis, sphincter of Oddi dysfunction, congenital anomalies such as pancreas divisum, annular pancreas, intraductal papillary mucinous neoplasia, occult malignancy, idiopathic chronic pancreatitis with ductal pathology such as stones or strictures, or anatomical causes such as choledochocele or anomalous pancreatico-biliary junction. An increasingly diagnosed cause of ‘unexplained’ pancreatitis is autoimmune, or lymphoplasmacytic sclerosing pancreatitis. Only the remainder with normal pancreatico-biliary ductal anatomy and no other etiology are appropriately labeled as ‘idiopathic’. Microlithiasis and occult gallstones Microlithiasis, biliary sludge, and occult gallstones are part of a spectrum of biliary disorders that may cause acute recurrent pancreatitis. The perceived prevalence of these disorders as a cause for recurrent pancreatitis, and the appropriate strategy for diagnosis and therapy, are the matter of some debate [37–39]. Patients with microlithiasis as a cause of pancreatitis usually have an intact gallbladder, and may or may not have associated abnormalities in liver chemistries. The best known study linking biliary sludge to recurrent pancreat- itis included many patients with fairly suggestive evidence of a biliary cause, such as visible sludge at ultrasonography or abnormal liver chemistries, and thus included patients whose pancreatitis would not be considered as ‘unexplained’ or ‘idiopathic’ in most centers [38]. Detecting microlithiasis Imaging techniques such as transcutaneous ultrasound may reveal layering sludge in the gallbladder or be entirely normal. Alternative diagnostic strategies include endoscopic ultrasound, which may be more sensitive for subtle gallbladder stone disease than transcutaneous ultrasound [40–43], and analysis of bile for crystals. Bile crystals Bile analysis may be performed directly on the bile duct aspirates via retrograde cannulation at ERCP [44], ideally after gallbladder contraction is induced with cholecystokinin, or on duodenal bile collected by tube or endo- scopy after gallbladder contraction is induced [45]. Bile is analyzed by a polariz- ing microscope for the presence of crystals. Problems with bile analysis include: (1) interobserver variation in technique and interpretation of analysis; (2) sensi- tivity and specificity of microscopic analysis for detecting biliary stone disease CHAPTER 9208 This is trial version www.adultpdf.com [46]; and (3) uncertain correlation between findings of bile abnormalities and response to therapeutic intervention such as cholecystectomy or biliary sphinc- terotomy [47]. In general, crystal analysis has been found to be of limited value with a very low prevalence after cholecystectomy [48,49]. Treatment of microlithiasis as a cause for acute pancreatitis can include cholecystectomy, endoscopic biliary sphincterotomy, or ursodeoxycholic acid [38,50]. Empiric cholecystectomy? In the patient with unexplained acute recurrent pan- creatitis and intact gallbladder, and normal pancreatico-biliary ductal anatomy by EUS or MRCP, it may be more prudent to consider empiric laparoscopic cholecystectomy rather than subjecting the patient to a potentially risky ERCP just to perform bile analysis of unclear predictive value. In patients who are postcholecystectomy, the low probability of a positive finding and high risk of performing ERCP just to make this diagnosis make the practice of bile analysis questionable. Other less invasive diagnostic modalities such as endoscopic ultrasound (EUS) or MRCP may be indicated prior to considering cholecystec- tomy as the diagnosis of occult tumors may otherwise be delayed. Sphincter of Oddi dysfunction Sphincter of Oddi dysfunction is thought by many to be an important cause of acute recurrent pancreatitis, accounting for up to one-third of otherwise unexplained cases [51,52]. Approaches to suspected sphincter of Oddi dysfunc- tion vary widely and are the subject of much controversy. This disorder is most often suspected as a cause of recurrent pancreatitis in women who are post- cholecystectomy, often with relatively mild pancreatitis and intermittent or con- tinuous abdominal pain between overt attacks of pancreatitis. Diagnosis of sphincter of Oddi dysfunction The diagnosis is generally based on findings of an abnormal sphincter of Oddi manometry with a basal pressure of greater than 40 mmHg [53–55]. A number of studies have demonstrated the discordance of manometric findings between the biliary and pancreatic sphincters, and thus stress the importance of assessing both sphincters [56–59] (Fig. 9.5). Endoscopic therapy for sphincter of Oddi dysfunction Although the traditional approach has been to perform biliary sphincterotomy or other biliary therapy to treat recurrent pancreatitis or other symptoms of sphincter of Oddi dysfunction [60–66], recent data suggest that combined ERCP IN ACUTE PANCREATITIS 209 This is trial version www.adultpdf.com pancreatic as well as biliary sphincterotomy, whether performed simulta- neously (Fig. 9.6) or sequentially (Fig. 9.7), is optimal to treat patients who have concomitant pancreatic sphincter hypertension [67]. The desired result is a ‘septotomy’ in which a ‘double-barrel’ appearance of the biliary and pancreatic sphincters is achieved (Fig. 9.8). In one study, biliary sphincterotomy alone resulted in improvement in only 25% of patients; in contrast, either sequential biliary and pancreatic sphincterotomy (78% response) or simultaneous dual sphincterotomy (82% response) resulted in significantly better outcomes [67]. Sphincterotomy without sphincter manometry? Some centers avoid sphincter of Oddi manometry or pancreatic endotherapy in these patients, advocating empiric biliary sphincterotomy [39,68] or alternative diagnostic tests such as quantitative scintigraphy [69], fatty-meal sonography, or secretin-stimulated assessment of pancreatic duct dilation [70]. Is sphincter manometry dangerous? This is based in part on the assumption that sphincter of Oddi manometry is the principal danger, and that merely avoiding this investigation will reduce risk [71]. The risk of any type of ERCP in these patients (women with recurrent abdominal pain and normal serum bilirubin) cannot be overemphasized; recent prospective multicenter multi- variate studies [16,17] have shown clearly that diagnostic ERCP or empiric biliary sphincterotomy carries a substantial risk of pancreatitis (approximately CHAPTER 9210 Common sphincter Biliary sphincter Pancreatic sphincter Fig. 9.5 Anatomy of the sphincter of Oddi including biliary, pancreatic, and common sphincters. This is trial version www.adultpdf.com 20% or higher), including the majority of severe and necrotizing cases. Newer techniques of aspirated sphincter manometry have been shown to add little or no independent risk to ERCP. Importantly, placement of a transpapillary pancreatic stent significantly reduces the risk of pancreatitis in patients with sphincter of Oddi dysfunction (from 27% to 7% in one randomized controlled trial) [72], and virtually eliminates the risk of severe post-ERCP pancreatitis (Fig. 9.9). Recent data suggest that, in patients with suspected sphincter of Oddi dysfunction, pancreatico-biliary manometry followed by combined pancreatico- biliary therapy that includes a pancreatic stent is actually safer than simple biliary sphincterotomy [73]. Prophylactic pancreatic stenting is now performed ERCP IN ACUTE PANCREATITIS 211 Fig. 9.6 Biliary and pancreatic sphincterotomies performed sequentially during the same procedure. This is trial version www.adultpdf.com CHAPTER 9212 Fig. 9.7 Pancreatic manometry and sphincterotomy in a patient unresponsive to previous biliary sphincterotomy. Fig. 9.8 Final appearance of pancreatic ‘septotomy’ after endoscopic biliary and pancreatic sphincterotomies for sphincter of Oddi dysfunction. This is trial version www.adultpdf.com routinely in many centers after pancreatic investigation in these types of patients [18,74,75]. Placement of pancreatic stents can range from technically easy (Fig. 9.10) to very challenging (Fig. 9.11) depending on pancreatic ductal anatomy and endoscopic expertise. Pancreatic stents have potential to cause damage, especially to normal ducts [76–78] (Fig. 9.12), and should be removed within 10–14 days from normal ducts. The trend is now to use smaller stents (3 or 4 Fr) compared with traditional larger (5–7 Fr) stents, because they are thought to cause less ductal injury and lower post-ERCP pancreatitis rates [79]. ERCP IN ACUTE PANCREATITIS 213 Cutting wire Papilloteme Guidewire Fig. 9.9 Schematic diagram of pancreatic stent placement to reduce risk of post-ERCP pancreatitis. Fig. 9.10 Relatively easy pancreatic ductal anatomy for placement of pancreatic stent. This is trial version www.adultpdf.com Many centers now use longer 3 Fr stents (8–12 cm long), without any internal flaps; most of these pass spontaneously in 1–3 weeks, and a simple abdominal radiograph is taken to confirm. This confers the same protection against pancre- atitis, and removes the need for a second procedure in most cases. Short (2 cm) straight stents may still be necessary for the 15% of patients with very tortuous small-caliber ducts, in whom passage of a guidewire to the tail may be difficult or impossible [80]. Without any type of pancreatic stent, however, available data suggest that the risk of empiric biliary sphincterotomy for suspected sphincter of Oddi dysfunction (about 25% pancreatitis) is about equal to its efficacy (approximately 25%). CHAPTER 9214 Fig. 9.11 Very difficult pancreatic ductal anatomy for placement of pancreatic stent. Fig. 9.12 Pancreatic stricture in a previously normal duct resulting from indwelling pancreatic stent for 4 weeks. This is trial version www.adultpdf.com Sphincter of Oddi dysfunction in patients with intact gallbladders Whether sphincter of Oddi dysfunction should be suspected in patients with an intact gallbladder is contentious. We generally recommend empiric cholecystec- tomy in most cases prior to investigation for sphincter of Oddi dysfunction as a cause for recurrent pancreatitis. Pancreas divisum Pancreas divisum is the most common congenital anomaly of the pancreas and may be present in up to 5% of the general population [81] (Figs 9.13 and 9.14). ERCP IN ACUTE PANCREATITIS 215 Common bile duct Minor papilla Major papilla Dorsal duct Ventral duct Fig. 9.13 Diagram of pancreas divisum. Fig. 9.14 Typical endoscopic appearance of major and minor papillae. This is trial version www.adultpdf.com [...]... pancreatitis Am J Med 2000; 109: 1 96 200 167 Gregor JC, Ponich TP, Detsky AS Should ERCP be routine after an episode of ‘idiopathic’ pancreatitis? A cost-utility analysis Gastrointest Endosc 19 96; 44: 118–23 168 Venu RP, Geenen JE, Hogan W, Stone J, Johnson GK, Soergel K Idiopathic recurrent pancreatitis: an approach to diagnosis and treatment Dig Dis Sci 1989; 34: 56 60 169 Binmoeller KF, Seifert H, Walter... recommend placement of a short-term pancreatic stent to reduce the risk of post -ERCP pancreatitis in this high-risk subgroup of patients with normal pancreatico-biliary ductal anatomy and recurrent pancreatitis (Figs 9.9–9.12) Because of the risk of ERCP, most authors recommend performance of ERCP only after two attacks of unexplained pancreatitis, unless the first is severe [125, 167 ] This dilemma can be... version www.adultpdf.com ERCP IN ACUTE PANCREATITIS imaging techniques, especially EUS and secretin-enhanced MRCP, provides more useful anatomic information, particularly regarding occult tumors, chronic pancreatitis [1 06] , occult biliary stone disease, and pancreas divisum, and in some cases eliminates the need for ERCP entirely [82, 160 ] In particular, the appropriateness of diagnostic ERCP and empiric biliary... Gastroenterology 19 96; 110: 1975–80 117 Binmoeller KF, Jue P, Seifert H et al Endoscopic pancreatic stent drainage in chronic pancreatitis and a dominant stricture: long-term results Endoscopy 1995; 27: 63 8–44 118 Cremer M, Deviere J, Delhaye M, Baize M, Vandermeeren A Stenting in severe chronic pancreatitis: results of medium-term follow-up in 76 patients Endoscopy 1991; 23: 171 6 119 Dumonceau JM,... 398A 68 Testoni PA, Caporuscio S, Bagnolo F, Lella F Idiopathic recurrent pancreatitis: long-term results after ERCP, endoscopic sphincterotomy, or ursodeoxycholic acid treatment Am J Gastroenterol 2000; 95: 1702–7 69 Kalloo AN, Pasricha PJ Therapy of sphincter of Oddi dysfunction Gastrointest Endosc Clin North Am 19 96; 6: 117–25 70 Di Francesco V, Brunori MP, Rigo L et al Comparison of ultrasound-secretin... trial version www.adultpdf.com 233 234 CHAPTER 9 65 Toouli J, Roberts-Thomson IC, Dent J, Lee J Sphincter of Oddi motility disorders in patients with idiopathic recurrent pancreatitis Br J Surg 1985; 72: 859 63 66 Wehrmann T, Seifert H, Seipp M et al Endoscopic injection of botulinum toxin for biliary sphincter of Oddi dysfunction Endoscopy 1998; 30: 702–7 67 Guelrud M, Plaz J, Mendoza S, Beker B, Rojas... protocol Gastrointest Endosc 1995; 42: 452 6 123 Smits ME, Badiga SM, Rauws EAJ, Tytgat GNJ, Huibregtse K Long-term results of pancreatic stents in chronic pancreatitis Gastrointest Endosc 1995; 42: 461 –7 124 Smits ME, Rauws EA, Tytgat GNJ et al Endoscopic treatment of pancreatic stones in patients with chronic pancreatitis Gastrointest Endosc 19 96; 43: 5 56 60 125 Ballinger AB, Barnes E, Alstead EM,... the ampulla of Vater Cancer 1989; 64 : 161 –7 145 Robertson JF, Imrie CW Acute pancreatitis associated with carcinoma of the ampulla of Vater Br J Surg 1987; 74: 395–7 1 46 Tham TC, Lichtenstein DR, Vandervoort J et al Pancreatic duct stents for ‘obstructive type’ pain in pancreatic malignancy Am J Gastroenterol 2000; 95: 9 56 60 147 Keeley SP, Freeman ML Placement of self-expanding metallic stents in the... Gut 1989; 30: 130–5 1 56 Gress F, Yiengpruksawan A, Sherman S et al Diagnosis of annular pancreas by endoscopic ultrasound Gastrointest Endosc 19 96; 44: 485–9 157 Lloyd-Jones W, Mountain JC, Warren KW Annular pancreas in the adult Ann Surg 1972; 1 76: 163 –70 158 Kochhar R, Nagi B, Chawla S et al The clinical spectrum of anomalous pancreatobiliary junction Surg Endosc 1989; 3: 83 6 This is trial version... in the detection of choledocholithiasis Clin Radiol 1999; 54: 60 4–14 165 Sherman S, Ruffolo TA, Hawes RH et al Complications of endoscopic sphincterotomy: a prospective series with emphasis on the increased risk associated with sphincter of Oddi dysfunction and nondilated bile ducts Gastroenterology 1991; 101: 1 068 –75 166 Froussard JL, Sosa-Valencia L, Amouyal G et al Usefulness of endoscopic ultrasonography . 19 86 3 2 100 0 a 475 Ligoury 19 86 24 8 63 0 a 0 a McCarthy 1988 21 19 89 0 a 0 a Lans 1992 30 10 90 0 a 0 a Lehman 1993 22 17 76 23 26 11 27 Coleman 1994 23 9 78 5 0 20 60 Sherman 1994 28 0 a 16. lower post -ERCP pancreatitis rates [79]. ERCP IN ACUTE PANCREATITIS 213 Cutting wire Papilloteme Guidewire Fig. 9.9 Schematic diagram of pancreatic stent placement to reduce risk of post -ERCP pancreatitis. Fig dysfunction [60 66 ], recent data suggest that combined ERCP IN ACUTE PANCREATITIS 209 This is trial version www.adultpdf.com pancreatic as well as biliary sphincterotomy, whether performed simulta- neously